4. DEFINITION
Localized area of ischemic necrosis in an
organ or tissue resulting most often from
reduction of arterial blood supply or
occasionally its venous
drainage………………….ROBBINS
5. ETIOLOGY
•Most Commonly,Infarcts are caused by Interruption in
arterial blood supply, called ischemic necrosis
•Less commonly,Venous obstruction can produce infarcts
termed stagnant hypoxia
6. •Generally,Sudden, complete and continuous occlusion by
thrombosis or embolism
•Torsion of a vessel, e.g. in testicular torsion
•Traumatic rupture or vascular compromise by edema, e.g.
anterior compartment syndrome.
• Nonocclusive circulatory insufficiency.
8. • Depending on Age
a.Recent or fresh.
b.Old or healed.
•Presence or absence of infection.
a.Bland – when free of bacterial contamination
b.Septic – when infected.
9. PATHOGENESIS
Localized hyperemia
Edema and hemorrhage
Cellular changes
Progressive proteolysis of necrotic tissue and lysis of red cells
An acute inflammatory reaction and hyperaemia
Blood pigments liberated by hemolysis
Progressive ingrowth of granulation tissue
10. PATHOLOGIC CHANGES
•Grossly, infarcts of solid organs -wedge-shaped
• apex -pointing towards occluded artery
wide base - on the surface of the organ.
•Infarcts due to arterial occlusion -pale
venous obstruction - hemorrhagic.
•Most infarcts become pale later as the red cell are lysed
but pulmonary infarcts never become pale due to
extensive amount of blood.
11. •Cerebral infarcts : poorly defined with central
softening (encephalomalacia).
•Recent infarcts : slightly elevated over the surface
• Old infarcts : shrunken , depressed under the surface
of the organ.
12. Microscopically
•The pathognomic cytologic change in all infarcts is
coagulative (ischaemic) necrosis of the affected area of
tissue or organ.
•In cerebral infarcts- characteristic liquefactive
necrosis.
13. At periphery of an infarct, inflammatory reaction is
noted.
Initially neutrophils predominate ,later macrophages and
fibroblasts appear.
Eventually, necrotic area is replaced by fibrous scar
tissue, may show dystrophic calcification.
In cerebral infarcts, the liquefactive necrosis is followed
by gliosis i.e. replacement by microglial cells distended
by fatty material (gitter cells).
14. INFARCTS OF DIFFERENT ORGANS
Location Gross
appearance
Outcome
1 Myocardial infraction Pale Frequently lethal
2 Pulmonary infraction Hemorrhagic Less commonly
fatal
3 Cerebral infraction Hemorrhagic &
Pale
Fatal if massive
4 Intestinal infraction Hemorrhagic Frequently lethal
5 Renal infraction Pale Not lethal unless
massive &
bilateral
6 Infract spleen Pale Not lethal
7 Infract liver Pale Not lethal
8 Infracts of lower extremity Pale Not lethal
15. LUNG INFARCTION
•Embolism of the pulmonary arteries
• May occur in patients who have inadequate circulation :
Chronic lung diseases
• Congestive heart failure.
16.
17. GROSS:
pulmonary infarcts : wedge-shaped
Base on the pleura,
hemorrhagic, variable in size
lower lobes.
Cut surface : dark purple
Shows blocked vessel near the apex of the infarcted area.
Old organized and healed pulmonary infarcts appear as
retracted fibrous scars.
18. Microscopically
• Characteristic histologic feature : coagulative
necrosis of the alveolar walls.
•Initially: infiltration by neutrophils and intense
alveolar capillary congestion hemosiderin,
phagocytes and granulation tissue.
19. KIDNEY INFARCTION
Renal infarcts are Common
caused by Thromboemboli
most commonly originating from heart
such as mural thrombi in the left atrium ,MI,Vegetative
endocarditis
Less commonly
renal artery atherosclerosis,
arteritis
sickle cell anemia.
20. Grossly:multiple and bilateral
Characteristically:wedge shape
Base - under capsule
Apex-pointing towards medulla
Narrow rim of preserved renal tissue is spared
Cut surface in first 2 to 3 days : red and congested
4th
day: centre
turns pale yellow.
1 week: typically anemic , depressed below
the surface
21. Microscopically
Characteristic:
affected area shows coagulative necrosis of
renal parenchyma i.e. ghosts of renal tubules and
glomeruli without intact nuclei and cytoplasmic content.
The margin of the infarct shows inflammatory reaction –
initially acute but later macrophages and fibrous tissue
predominate.
22. INFARCT SPLEEN
•Common site for infarcts
•It results from Occlusion of one of the splenic arteries or
its branches.
Most common cause : thromboemboli arising in heart
(eg.mural thrombi in the left atrium
vegetative endocarditis
myocarditis
myocardial infarction)
23. •Less frequently by obstruction of microcirculation (e.g.
in myeloproliferative diseases, sickle cell anemia,
arteritis, Hodgkin's disease, bacterial infections).
•Grossly, splenic infarcts are often multiple.
•Characteristically pale or anemic, wedge-shaped
• base - at the periphery
• apex -pointing towards hilum.
24. •Features are similar to those found in anemic infarcts in
kidney.
•Coagulative necrosis and inflammatory reaction are
seen.
•Later, the necrotic tissues is replaced by shrunken
fibrous scar.
MICROSCOPICALLY
25. INFARCT LIVER
• Uncommon
• Dual blood supply
•Obstruction of the portal vein is usually secondary to
other diseases : Hepatic cirrhosis,
IV invasion of primary CA of liver,
CA of pancreas
• Generally does not produce ischemic infarction but
instead reduced blood supply to hepatic parenchyma
causes non-ischemic infarct called infarct of Zahn.
26. •Obstruction of the hepatic artery or its branches:
arteritis, arterio-sclerosis, bland or septic emboli.
•Grossly, anemic but sometimes hemorrhagic due to
stuffing of the site by blood from the portal vein.
•Infarcts of Zahn (non-ischemic infarcts) produce sharply
defined red-blue area in liver parenchyma.
27. Microscopically
Infarcts of Zahn occurring due to reduced portal blood
flow result in atrophy of hepatocytes and dilatation
of sinusoids .
28. CEREBRAL INFARCTION
•Local vascular occlusion
•Occasionally,
non-occlusive cause
compression of the cerebral
arteries from outside
and from hypoxic
encephalopathy.
29. •Clinically, the signs and symptoms depend upon the
region infarcted.
•In general, the focal neurologic deficit termed stroke, is
present.
•However, significant atherosclerotic cerebrovascular
disease may produce transient ischemic attacks (TIA).
30. ARTERIAL OCCLUSION
•Occlusion of the cerebral arteries by thrombi- common
•Embolic arterial occlusion is commonly derived from the
heart
mural thrombosis complicating MI
arterial fibrillation and endocarditis.
31. VENOUS OCCLUSION
• Infrequent phenomenon due to good communications
of the cerebral venous drainage.
•However in cancer, due to increased predisposition to
thrombosis, superior sagittal thrombosis may occur
leading to bilateral, parasagittal, multiple hemorrhagic
infarcts.
33. PATHOLOGIC CHANGES
• Anemic or hemorrhagic
• Affected area : soft and swollen
blurring of junction between grey
and white matter.
34. •Within 2-3days, the infarct undergoes softening and
degeneration.
• Central liquefaction with peripheral firm glial reaction
• thickened leptomeninges, forming a cystic infarct.
• Hemorrhagic infarct : red and superficially resembles a
hematoma
35.
36.
37. MYOCARDIAL INFARCTION
Most Important consequence of coronary
artery disease
Patient may die within first few hours of the
onset while remainder suffer from effects of
cardiac function
INCIDENCE:Occurs at all age but more
common in elderly.
38. PREDISPOSING FACTORS FOR
CORONARY ARTHEROSCLEROSIS
Hyperlipidaemia
Hypertension
DM
Cigarette smoking etc
DOCUMENTED WELL BY AUTOPSY STUDIES
AND CORONARY ANGIOGRAPHIC STUDIES.
39. ETIOPATHOGENESIS
1.Mechanism of myocardial ischemia
2.Role of platelets
3.Complicated plaques
4.Non – atherosclerotic causes
5.Transmural versus subendocardial infarcts
40. MECHANISM OF
MYOCARDIAL ISCHEMIA
DIMINISHED CORONARY
BLOOD FLOW
Coronary artery
disease,shock
•MYOCARDIAL
OXYGEN DEMAND
•Exercise,emotion
HYPERTROPHY OF HEART
W/O SIMULTANEOUS
INCREASE IN CORONARY
BLOOD FLOW
Hypertension,Valvular heart
disease
41. ROLE OF PLATELETS
•Rupture of atherosclerotic plaque exposes : sub
endothelial collagen to platelets which undergo
aggregation, activation & release reaction.
•These events contribute to the build up of the platelet
mass that gives rise to emboli or initiate thrombosis.
42. COMPLICATED PLAQUES
Two complications occur
Superimposed coronary thrombosis – seen in about half of the cases
of acute MI. Infusion of fibrinolysins in the first few hours of
development of acute MI in such cases restores blood flow in the
blocked vessel in majority of cases.
Intramural hemorrhage – is found in about one third of cases of acute
MI. Hemorrhage and thrombosis may occur together in some cases.
44. 1
Feature Transmural infract Subendoc
ardial
infarct
1 Definition Full-thickness, solid Inner third to
half, patchy
2 Frequency Most frequent (95%) Less frequent
3 Distribution Specific area of coronary
supply
Circumferent
ial
4 Pathogenesis > 75% coronary stenosis Hypoperfusio
n of
myocardium
5 Coronary
thrombosis
Common Rare
6 Epicarditis Common None
45. LOCATION OF INFARCTS
• LV
•RV is less susceptible , due to its thin wall, having less
metabolic requirements and is thus adequately nourished
•Atrial infarcts, whenever usually accompany infarct of LV
•LA is relatively protected because it is supplied by oxygenated
blood in the left atrial chamber.
46. REGION OF INFARCTION
Area of obstructed
blood supply by one or more
of three coronary arterial
trunks in descending order:
1.Left anterior descending
coronary artery :40 to 50%
2.Right coronary artery :30 to 40%
3.Left circumflex coronary
artery:15 to 20%
47. 3 Regions of myocardial infraction.
Stenosis of the left anterior descending
coronary artery is the most common (40-
50%).
Region of infarction in the anterior part of the
left ventricle including the apex and the
anterior two-thirds of the interventricular
septum.
48. Stenosis of the right coronary artery
is the next most frequent (30-40%) .
It involves the posterior part of the
left ventricle and the posterior one-
third of the interventricular septum.
49. Stenosis of the left circumflex
coronary artery is seen least
frequently (15-20%).
Its area of involvement is the lateral
wall of the left ventricle.
50. 50
Microscopically
The changes are similar in both transmural and
subendocardial infracts.
There is ischemic coagulative necrosis of the
myocardium which eventually heals by fibrosis.
However, sequential microscopic changes are
observed.
51. REFERENCES
1.Robbins and Cotran - Pathologic basis of
diseases. 8th
edition.
2. Harsh Mohan – Text book of pathology. 3rd
edition.
3.Mc Gee, Isaacson and Wright – Oxford text
book of Pathology. Principles of Pathology
volume 1.
4.Anderson’s Pathology – 10th
edition
is the process of tissue necrosis resulting from some form of circulatory insufficiency; the localized area of necrosis so developed is called an infarct.
A compartment space is anatomically determined by an unyielding fascial (and osseous) enclosure of the muscles. The anterior compartment syndrome of the lower leg (often referred to simply as anterior compartment syndrome), can affect any and all four muscles of that compartment: tibialis anterior, extensor hallucis longus, extensor digitorum longus, and peroneus tertius..incomplete arthersclerotic narrowing of coronary arteries produces mi.
This term is often mistakenly used to describe various related/proximal conditions, including Anterior Shin Splints. It is important to distinguish between the two, as shin splints rarely causes serious health problems, while Anterior Compartment Syndrome can lead to irreversible damage.
The true compartment syndrome arises due to increased pressure within the unyielding anterior compartment of the leg. The pressure obstructs venous outflow, which causes further swelling and increased pressure. The resultant ischemia leads to necrosis (death of tissue) of the muscles and nerves. The process can begin with swelling of the tibialis anterior, extensor hallucis longus, extensor digitorum longus, and/or the peroneus tertius muscles in response to strong eccentric contractions sufficient to produce postexercise soreness.
Symptoms
Diffuse tightness and tenderness over the entire belly of the tibialis anterior that does not respond to elevation or pain medication can be early warning signs and suggestive of Anterior Compartment Syndrome. Other common symptoms include excessive swelling that causes the skin to become hot, stretched and glossy. Pain, paresthesias, and tenderness in both the ischemic muscles and the region supplied by the deep common fibular nerve are exhibited by patients suffering from this condition. Sensitivity to passive stretch and active contraction are common, and tend to increase the symptoms.
Diagnosis
If these symptoms are observed/experienced it is important to contact a physician specializing in sports medicine (MD/DO), a doctor of podiatric medicine (DPM), or other qualified health care professional immediately so as to get the appropriate advice/treatment before serious damage occurs.
The 5 Ps of Anterior Compartment Syndrome:
Pain
Pallor
Paresthesia
Pulselessness
Paralysis (If not treated)
arterial occlusion,compact organs.Kidney,heart ,spleen. –venous occlusion seen in soft loose tissues and are caused either by pulmonary arterial obstruction, e.g. in the lungs ,intestine
or by arterial or venous occlusion, e.g. in the intestines.
Pale infarcts r due to arterial obstruction in solid organs n red due to venous n loose tissues
Local anoxaemia occurs immediately after obstruction of the blood supply.
Within few hours the affected part becomes swollen due to oedema and haemorrhage, amount is veriable, being more marked in the lungs and spleen, and less extensive in the kidneys and heart.
Cellular changes such as cloudy swelling and degeneration appears early, while death of the cells or necrosis occurs in 12-48hours.
There is progressive autolysis of the necrotic tissue and haemolysis of the red cells.
Inflammatory reaction and hyperaemia appear at the same time in the surrounding tissues in response to products of autolysis.
Blood pigments, hematoidin and haemosiderin, liberated by haemolysis are deposited in the infract. At this stage most infracts becomes pale due to loss of red cells.
Following this, there is progressive ingrowth of granulation tissue from the margin of the infract so that eventually the infract is replaced by a fibrous scar. Dystrophic calcification may occur sometimes. However, in the case of infract brain, there is liquefactive necrosis which heals by gliosis.
DIAGRAM REPRESENTS GRANULATION TISSUE
Diagram- cerebral infarct
however, there is giagram represents – liquefactive necrosis
arteries may produce pulmonary infarction, though not always. This is because the lungs receive blood supply from bronchial arteries as well, and thus occlusion of pulmonary artery ordinarily does not produce infarcts.
Arrow represents wedge shaped
Later place is taken by
Found in 5%of autopsies. originating from the heart such as in
Because it draws its blood supply from under the capsule.
Pointing towards
Just as in lungs, infracts in the liver are uncommon due to dual blood supply – from portal vein and from hepatic artery. Occlusion of portal vein or its branches
Infracts of Zahn (non-ischemic infracts) produce sharply defined red-blue area in liver parenchyma.
Arterial or venous. Occasionally, it may be the result of non-occlusive cause such as compression of the cerebral arteries from outside and from hypoxic encephalopathy.
Thrombotic occlusion of the cerebral arteries is most frequently the result of atherosclerosis, and rarely, from arteries of the cranial arteries.
Thrombotic occlusion of the cerebral arteries is most frequently the result of atherosclerosis, and rarely, from arteries of the cranial arteries.
Grossly, an anemic infract becomes evident 6-12hrs after its occurrence.
Hemorrhagic infract : red and superficially resembles a hematom, it is usually a result of fragmentation of occlusive arterial emboli or venous thrombosis.lt of fragmentation of occlusive arterial emboli or venous thrombosis.
Initially, eosinophilic neuronal necrosis and lipid vacuolization produced by breakdown of myelin.
Simultaneously, the infracted area is infiltrated by neutrophils
2. After the first 2-3days, there is progressive invasion by macrophages and there is astrocytic and vascular proliferation.
3. In the following weeks to months, the macrophages clear away the necrotic debris by phagocytosis followed by reactive astrocytosis, often with little fine fibrosis.
A hemorrhagic infract has some phagocytes containing haemosiderin.
4. Ultimately, after 3-4 months and old cystic infract is formed which shows a cyst transversed by small blood vessels and has peripheral fibrillary gliosis.
Small cavitary infracts are called lacunar infracts and are commonly found as a complication of systemic hypertension.
Region of infraction depends upon the area of obstructed blood supply by one or more of three coronary arterial trunks,
